Li et al. using another sepsis model, the acute pancreatitis model, revealed that LTB4 production promoted PMN rM, and this effect was mediated by substance P. Substance P treatment increase phosphorylation of protein kinase C (PKC) α and mitogen- activated protein kinases (MAPKs), which further promoted LTB4 production. The gene discussed is TAC1; the disease is acute pancreatitis.